Equine Herpesvirus type 1 (EHV-1) is one of the most important and prevalent pathogens of equine populations worldwide (Ma et al., J. of General Virology 91, 1817-1822, 2010). Together with its close relatives varicella-zoster virus, bovine Herpesvirus type 1, pseudorabies virus and EHV-4, EHV-1 forms the genus Varicellovirus in the subfamily Alphaherpesvirinae of the family Herpesviridae of the order Herpesvirales (Davison et al., The order Herpesvirales. Arch Virol 154, 171-177, 2009). Diseases caused by EHV-1 range from mild rhinopneumonitis and abortion in pregnant mares to neurological disease that is frequently lethal in affected horses (Allen et al., Prog Vet Microbiol Immunol 2, 78-144, 1986; Carroll et al., Aust Vet J 62, 345-346, 1985; Crabb et al., Adv Virus Res 45, 153-190, 1995). The pathogenesis of EHV infection is very complex. Natural infection occurs through inhalation or ingestion of the infectious virus. Within a few days of the virus can be found in leucocytes, where it is protected from recognition and attacks by the immune system. The virus disseminates via cell-associated viremia to secondary sites of replication (Allen et al., Proceedings 8th Equine Infectious Disease Conference, Dubai 23-26, pp 129-146, 1998).
EHV-1 harbors a 150 kb double-stranded DNA genome that is highly conserved among strains. A neuropathogenic strain Ab4 (GenBank accession No. AY665713) and a nonneuropathogenic strain V592 (GenBank accession No. AY464052) were extensively characterized and showed a nucleotide variation rate of approximately 0.1% (Nugent et al., J. Virol 80, 4047-4060, 2006). It was found that only a minority of EHV-1 strains are capable of inducing neurological disorders, although all strains can cause respiratory disease and abortion (Mumford et al., J. Reprod Fertil Suppl 35, 509-518, 1987; Ostlund, Vet Clin North Am Equine Pract 9, 283-294, 1993; Wilson, Vet Clin North Am Equine Pract 13, 53-72, 1997). Recently, epidemiological as well as reverse-genetic studies have shown that a single-nucleotide polymorphism at position 2254 (G/A2254) of open reading frame 30 (ORF30), encoding viral DNA polymerase (Pol), will lead to a variation at the amino acid position 752 (D/N752), which is associated with the virus's neuropathogenic potential (Goodman et al., J Biol Chem 281, 18193-18200, 2007; Van de Walle et al., J. Infect Dis 200, 20-25, 2009; Smith et al., Vet. Microbiol., 141, 5-11, 2010). It has been shown that residue 752 in the essential Pol of EHV-1 is not required for virus growth and that the N752 mutation confers a drug-sensitive phenotype to the virus (Ma et al., 2010).
Glycoprotein C (gC) of EHV-1 was shown to play important role in the early steps of infection and in release of virions (Osterrieder, Virus Research 2, 165, 1999). Glycoprotein C of EHV-1 is non-essential for virus growth. It mediates primary attachment, and is required for efficient virus replication in primary equine cells (Osterrieder, 1999).
Conventional killed vaccines provide only partial clinical and virological protection against respiratory infections, but do not prevent cell-associated viremia. Considering the susceptibility of animals, including humans, to herpesvirus, a means of preventing herpesvirus infection and protecting animals is essential. Accordingly, there is a need for an effective vaccine against herpesvirus.
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